Survival of the Sickestby Dr. Sharon Moalem & Jonathan Prince Post #1
“In a nonhemochromatic person, macrophages have plenty of iron. Many infectious agents, like tuberculosis, can use that iron within the macrophage to feed and multiply... If your macrophages lack iron, as they do in people who have hemochromatosis, those macrophages have an additional advantage – not only do they isolate infectious agents and cordon them off from the rest of the body, they also starve those infectious agents to death” (Moalem 13).
A macrophage is a phagocytic leukocyte that extends pseudopodia to engulf and destroy invading microorganisms. It is part of the body’s innate immunity, which produces rapid responses to a broad range of microbes. Macrophages are involved in internal defense, which comes into play if an invading pathogen is able to bypass the external defenses (such as skin, mucous membranes, and secretions). The process by which a macrophage ingests pathogens is depicted in the diagram below (1):
As the excerpt highlights, one of the greatest flaws in a normal macrophage is its abundance of iron. Iron is essential for virtually all life on earth, and as a result, human blood and tissue are an “iron gold mine” for bacteria, fungi, and protozoa (2). This becomes a problem when a normal macrophage ingests infectious agents. If the invaders have the ability to access iron within the macrophage, they will be able to grow stronger and multiply rapidly. Clearly, this is counter-productive to the macrophage; in an attempt to protect the body, it only strengthens the pathogens. However, hemochromatic macrophages are deficient in iron. By limiting the availability to iron, these macrophages are better equipped to subdue potentially harmful microorganisms. In fact, research has demonstrated that hemochromatic macrophages are significantly better at destroying bacteria than nonhemochromatic macrophages.
The evidence presented in the excerpt suggests that evolution played a large role in the proliferation of hemochromatosis. Because hemochromatic individuals were better equipped to combat pathogens, they were less vulnerable to epidemics such as the Bubonic Plague. In accordance with natural selection, people with hemochromatosis were more likely to survive, and therefore more likely to reproduce and pass the trait on. Over time, human beings in Europe may have evolved to carry hemochromatosis in response to the Bubonic Plague.
Dr. Sharon Moalem has a unique perspective on disease, which he reveals in his discussion about the origin of hemochromatosis. I find it very interesting to read about his theories and the evidence he has to support them. It’s fascinating to learn not just the scientific reasoning of how inherited diseases come about, but why they developed in the first place.
Works Cited:
1. Campbell, Neil A., and Jane B. Reece. Biology AP Edition. Upper Saddle River: Prentice Hall College Div, 2004. Print.
2. Moalem, Sharon, and Jonathan Prince. Survival of the Sickest. New York: William Morrow, 2007. Print.
Post #2
“Cholesterol is required to make and maintain cell membranes. It helps the brain to send messages and the immune system to protect us against cancer and other diseases. It’s a key building block in the production of estrogen and testosterone and other hormones” (Moalem 51).
Cholesterol is a type of steroid, which by definition, is a “lipid characterized by a carbon skeleton consisting of four fused rings” (1). Relating to the fluid mosaic model that we learned about in the beginning of the year, one of its main functions is to maintain membrane fluidity at different temperatures. It reduces membrane fluidity by decreasing phospholipid movement at moderate temperatures, but also hinders solidification by disrupting the packing of phospholipids at low temperatures (1). For this reason, cholesterol is a vital component of animal cell membranes.
Cholesterol also has a crucial role in the endocrine system. Since cholesterol is a lipid, it is hydrophobic and can easily diffuse through the phospholipid bilayer of a plasma membrane. Once it enters the target cell, it binds to an intracellular receptor either in the cytoplasm or nucleus. Typically, the hormone-receptor complex acts as a transcription factor and activates the expression of certain genes. The process is summarized in the diagram below (2):
In order for the hormone to create a protein, transcription and translation must occur. In transcription, the DNA molecule unwinds and, using one of the DNA strands as a template, RNA polymerase creates a complementary strand of RNA. It does so by pairing the nucleotides A=U, T=A, G=C and C=G. After, the new RNA strand is transported from the nucleus to a ribosome. In translation, each sequence of three nucleotides is grouped into a codon. tRNA molecules, each with a complementary anti-codon, retrieve the appropriate amino acid from the cytoplasm and carry it to the ribosome. This is done for each codon until a stop codon is reached, and a peptide is formed. The peptide is then released into the cytoplasm (1).
This excerpt connects to the theme of the relationship of structure to function. As mentioned before, cholesterol is a lipid and is hydrophobic. Therefore, it is able to cross the hydrophobic layer of a target cell’s plasma membrane. Cholesterol’s ability to penetrate the plasma membrane of a target cells allows it to serve as a precursor for multiple other hormones in the endocrine system. In addition, the receptor that a lipid-based hormone binds to is shape-specific. As a result, only specific hormones can bind to the receptors (1).
In Chapter 3, Dr. Sharon Moalem discusses the connection between sunlight and cholesterol. It makes sense that he does not go into very much detail regarding the specifics of cholesterol, because that would detract from his point. He presents strong evidence that high cholesterol found in African Americans is an evolutionary adaptation that is no longer needed, but the end of his chapter really bothers me. He states, “If you knew that you might be able to reduce your excess cholesterol by getting enough sunlight to convert it to vitamin D, wouldn’t you rather hit the tanning salon before starting a lifetime of Lipitor?” (Moalem 70). He supports this statement by stating that cholesterol-reducing drugs, such as Lipitor, can have serious side effects. When I researched this, however, I learned that serious side effects are extremely rare, and that drugs such as Lipitor generally cause more good than they do harm (4). At the same time, indoor tanning has a direct link to the premature development of skin cancer, and its effects can be devastating (3). So no, actually. I would rather have high cholesterol at the age of fifty than die of skin cancer before I turn seventeen.
Commentary 1 (H.K.)
I agree with Margaret's statement about cholesterol-lowering drugs not having as serious side effects on the people that consume them. For example, I know my cousin has been taking the drug Niacin, which lowers the LDL (bad cholesterol) and raises the HDL (good cholesterol), and has experienced no side effects what so ever of this drug. Even though though Niacin has minor side effects like itching of skin and headaches, my cousin has not been affected by any of them. There are many other drugs out there designed to lower cholesterol, who people claim to be are really "dangerous" to the health because of their serious side effects. But the chances of one experiencing the side effects is very low, and it would be a smart idea to take the drug to improve ones health then to worry about it's side effects which rarely occur.
Commentary 1 (KB)
I also think that it is interesting that something that is so useful in so many ways (cholesterol is a key building block and a staple in cell structure) has such a bad reputation. Excess cholesterol is definitely a problem, but I think that Moalem is looking at it the wrong way. My dad's been on Lipitor for a while (high cholesterol/heart problems run on both sides of my family) with no side effects, so I agree with Margaret and Hira that side effects are very rare. However, a recent issue of 17 Magazine did a spread on tanning and using a tanning bed once could increase your risk for melanoma by 75%! (1) But at least you'll be cholesterol free, and have enought vitamin D.
The point I'm trying to make is that there are tradeoffs with everything in life and simply going tanning is a friviolous and dangerous way to suggest that people limit their cholesterol. There are other, safer ways to do it--limiting unhealthy food, getting healthy sun exposure (perhaps while outside exercising) and when genetics really are stacked against you, medicine should be between you and your private physician, not someone who's just writing a book. Different medicines work differently for people (as Dr. Moalem stated in the chapter on methylation) and therefore side effects manifest themselves differently. And lots of the side effects on commericals (severe dehydration, dizziness, loss of limbs, maybe even death) are really probably put in there by lawyers trying to cover themselves in the event that a doctor misprescribes something, or the medicine really does disagree with the patient. Using a medicine correctly when there is a legitimate need should never be frowned upon, especially by a doctor who doens't know the patient's medical history. My dad's uncle died at fifty from a heart attack. And who knows? Maybe Lipitor (along with diet/exercise) is what kept him from having one, too.
Works Cited
"The Tan You Could Be Risking Your Life For." Seventeen May 2010: 80. Print.
Post #3
“The gene that is responsible for G6PD protein production – or deficiency – goes by the same name, G6PD. Because the gene for G6PD deficiency is carried on the X chromosome, the condition is much more common in men… There are more than 100 possible mutations of this gene, but they fit into two major categories, one that arose in Africa, called GdA-, and one that arose around the Mediterranean, called GdMed. These mutations cause serious problems only when free radicals start overwhelming your red blood cells and there isn’t enough G6PD to clean them up” (Moalem 75-76).
In mammals, there are two types of sex chromosomes: X and Y. Humans with two X chromosomes (XX) are female, and humans with one X and one Y chromosome (XY) are male. During meiosis, the two sex chromosomes separate and each gamete receives one. Therefore, each ovum contains an X chromosome, while each sperm can contain either an X or a Y chromosome. When fertilization occurs, the zygote receives one X chromosome from its mother and either an X or Y chromosome from its father. As a result, mothers can pass X-linked alleles to their daughters (XX) and sons (XY), and fathers can pass X-linked alleles only to their daughters (XX). In the case of the G6PD, the gene that is responsible for the G6PD-deficiency is a recessive X-linked gene. This means that females must have two mutated X chromosomes to have a G6PD-deficiency, while males only need one mutated X chromosome (1). Consequently, males are much more likely to exhibit a G6PD-deficiency.
Mutations can arise from base substitutions and gene rearrangements. Also known as point mutations, base substitutions occur when one nucleotide base is substituted for another. They can result in nonsense mutations, which cause the premature termination of protein translation; missense mutations, in which a codon is altered and produces a different amino acid; and silent mutations, which cause no detectable change in the corresponding protein sequence. In addition to that, there are five main types of gene rearrangements:
1. A deletion occurs when a chromosomal segment is lost
2. An insertion occurs when a segment is inserted into the chromosome
3. A duplication occurs when a segment is repeated
4. An inversion occurs when a segment reverses within a chromosome
5. A translocation occurs when a segment is moved from one chromosome to a nonhomologous chromosome. In a reciprocal translocation, the nonhomologous chromosomes exchange fragments. In a nonreciprocal translocation, a chromosome loses a fragment without receiving a fragment in return.
More often than not, a chromosomal alteration changes the protein sequence, which changes the expression of a certain gene (1). These events can give rise to mutations such as the G6PD-deficiency gene.
The theme of continuity and change states that all living things pass down genetic information between generations to maintain the species, but there are mechanisms that can lead to change over time. It connects to the excerpt in the way that the G6PD-deficiency gene has been passed from generation to generation on the X chromosome. While males are more likely to have a G6PD deficiency, females can serve as carriers. Also, mutations resulting from base substitutions or gene rearrangements can lead to mutations such as the G6PD-deficiency gene.
Something I thought was very interesting about this chapter (IV: Hey Bud, Can You Do Me a Fava?) was that many plants that I consume have toxins in them. Dr. Sharon Moalem states, “What’s more surprising is why we continue to cultivate and consume thousands of plants that are toxic to us. The average human eats somewhere between 5,000 and 10,000 natural toxins every year. Researchers estimate that nearly 20 percent of cancer-related deaths are caused by natural ingredients in our diet” (Moalem 83). Somewhat recently, natural and organic food has been gaining popularity. I found it surprising to learn that the “healthy” foods can actually be harmful; for example, the psoralen found in celery can cause skin damage (Moalem 87). I guess it could have been expected, since plants must have evolved defenses to protect themselves from predation, but I still find it rather depressing.
Works Cited:
1. Campbell, Neil A., and Jane B. Reece. Biology AP Edition. Upper Saddle River: Prentice Hall College Div, 2004. Print.
2. Moalem, Sharon, and Jonathan Prince. Survival of the Sickest. New York: William Morrow, 2007. Print.
Post #4
“Most of these microbes are found in the digestive system, where they play crucial roles. These intestinal bacteria, or gut flora, help to create energy by breaking down food products we otherwise couldn’t break down; they help to train our immune systems to identify and attack harmful organisms; they stimulate cell growth; and they even protect us against harmful bacteria” (Moalem 98).
The large intestine of a human is mainly responsible for the reabsorption of water, and is one of the last stages of the digestive process. However, it also contains approximately 100 trillion microorganisms. These microorganisms are mostly harmless bacteria, and live on unabsorbed organic material in the large intestine. Some of the bacteria produce vitamins - such as biotin, folic acid, and vitamin K – that are absorbed into the blood to supplement our dietary intake of vitamins (1). Other bacteria digest polysaccharides for which we have no enzymes, and stimulate the development of the adaptive immune system (2).
Symbiosis is defined as “an ecological relationship between organisms of different species that are in direct contact” (2). It can exist in various forms. In mutualism, both symbiotic organisms benefit. This excerpt provides an excellent example of mutualism; the bacteria living in the digestive system synthesize vitamins, digest polysaccharides, and stimulate the development of the adaptive immune system (1). In return, they are provided with food. In this way, both organisms are able to benefit from the relationship.
In commensalism, one organism benefits while the other is neither helped nor harmed. For example, remoras form temporary attachments onto sharks. When the shark feeds, the remoras consume the scraps. The shark is unaffected by this relationship.
In parasitism, one organism benefits at the expense of the other. A parasite is an organism that “lives on or in the body of another organism (the host), from whose tissues it gets its nourishment and to whom it does some damage” (2). The parasite is able to harm its host either by consuming its tissues or liberating toxins. In addition, the relationship between a parasite and its host can range from “hit and run,” in which the parasite lives in the host for a brief period before moving on to another, and parasites that establish chronic infections. For animals, parasites can come in the form of viruses, bacteria, fungi, protozoans, flatworms, nematodes, insects (e.g. lice) and arachnids (mites) (2).
This excerpt connects to the theme of interdependence in nature. As symbiosis demonstrates, living organisms rarely exist alone in nature. In the case of the intestinal bacteria found in humans, both organisms are able to benefit from one another. There are countless interactions between species that occur on multiple levels, and symbiosis is just one of them.
Something that I learned from researching this topic was that as by-products of their metabolism, many intestinal bacteria generate gases, including methane and hydrogen sulfide. Then, I was able to recall a song that everyone cool used to sing, and it went along the lines of “BEANS, BEANS, THE MAGICAL FRUIT. THE MORE YOU EAT, THE MORE YOU TOOT…” This led me to wonder: do beans make these bacteria more active, therefore causing people to toot more? It turns out I was right, and I even have a link full of additional fascinating information: http://www.heptune.com/farts.html
“The prospect of programmed aging opens up the door to all kinds of exciting possibilities. Already, scientists are exploring benefits that may be found by turning aging mechanisms off – and by turning them back on. The possibility of short-circuiting telomerase in cancer cells – the enzyme that cancer cells use to make themselves immortal – may lead to powerful new weapons against cancer” (Moalem 191).
The semiconservative model states that when a double helix replicates, each of the two daughter molecules will have one old strand and one newly made strand. DNA replication begins when helicase unwinds the DNA molecule. DNA polymerase binds complementary nucleotide bases to the template strand (Adenine=Thymine, Cytosine=Guanine). However, DNA polymerase can only add nucleotides in a 5’ to 3’ direction (the leading strand). As a result, RNA primase must be used to start Okazaki fragments on the lagging strand, which runs in a 3’ to 5’ direction. For linear DNA, the RNA primer on the lagging strand can be removed but cannot be replaced with DNA. For this reason, repeated rounds of replication produce shorter and shorter DNA molecules (3).
To protect against the possible loss of genes at the end of chromosomes, eukaryotic cells have telomeres. Telomeres are nonsense nucleotide sequences at the end of chromosomes that repeat thousands of times. An enzyme called telomerase catalyzes the lengthening of telomeres after DNA replication to ensure that the gene-containing portion is not removed (2).
Cancer cells generally exhibit abnormally high levels of telomerase activity. Because the telomerase is able to quickly restore telomeres, cancer cells are capable of unlimited cell division. In this way, they are essentially immortal. This relates to the theme of science, technology, and society. Advances in technology have led to the discovery of telomerase, which can be applied to cancer research and other fields. In turn, this will greatly benefit society. It is estimated that 1,529,560 people in the United States will develop cancer in 2010, and new discoveries in science will have an enormous impact on society (1).
In this excerpt, Dr. Sharon Moalem writes that the prospect of telomerase “opens the door to all kinds of exciting possibilities.” He basically says that researchers will be able to kill two birds (aging and cancer) with one stone. The shortening of telomeres is believed to be one of the main causes of aging, because it often leads to apoptosis (also referred to as cell suicide). At the same time, the continuous restoration of telomeres is believed to be one of the main causes of cancer. Without a doubt, it will be difficult to cure one problem without affecting the other, and I believe that Dr. Sharon Moalem oversimplifies the complications associated with telomerase research. It is also possible that he is extremely optimistic. Works Cited
1. Campbell, Neil A., and Jane B. Reece. Biology. San Francisco: Benjamin Cummings, 2002. Print. 2. "Cancer Statistics for 2010." American Cancer Society. Web. 13 June 2010. <http://www.cancer.org/docroot/stt/stt_0.asp>.
Post #1
“In a nonhemochromatic person, macrophages have plenty of iron. Many infectious agents, like tuberculosis, can use that iron within the macrophage to feed and multiply... If your macrophages lack iron, as they do in people who have hemochromatosis, those macrophages have an additional advantage – not only do they isolate infectious agents and cordon them off from the rest of the body, they also starve those infectious agents to death” (Moalem 13).
A macrophage is a phagocytic leukocyte that extends pseudopodia to engulf and destroy invading microorganisms. It is part of the body’s innate immunity, which produces rapid responses to a broad range of microbes. Macrophages are involved in internal defense, which comes into play if an invading pathogen is able to bypass the external defenses (such as skin, mucous membranes, and secretions). The process by which a macrophage ingests pathogens is depicted in the diagram below (1):
As the excerpt highlights, one of the greatest flaws in a normal macrophage is its abundance of iron. Iron is essential for virtually all life on earth, and as a result, human blood and tissue are an “iron gold mine” for bacteria, fungi, and protozoa (2). This becomes a problem when a normal macrophage ingests infectious agents. If the invaders have the ability to access iron within the macrophage, they will be able to grow stronger and multiply rapidly. Clearly, this is counter-productive to the macrophage; in an attempt to protect the body, it only strengthens the pathogens. However, hemochromatic macrophages are deficient in iron. By limiting the availability to iron, these macrophages are better equipped to subdue potentially harmful microorganisms. In fact, research has demonstrated that hemochromatic macrophages are significantly better at destroying bacteria than nonhemochromatic macrophages.
The evidence presented in the excerpt suggests that evolution played a large role in the proliferation of hemochromatosis. Because hemochromatic individuals were better equipped to combat pathogens, they were less vulnerable to epidemics such as the Bubonic Plague. In accordance with natural selection, people with hemochromatosis were more likely to survive, and therefore more likely to reproduce and pass the trait on. Over time, human beings in Europe may have evolved to carry hemochromatosis in response to the Bubonic Plague.
Dr. Sharon Moalem has a unique perspective on disease, which he reveals in his discussion about the origin of hemochromatosis. I find it very interesting to read about his theories and the evidence he has to support them. It’s fascinating to learn not just the scientific reasoning of how inherited diseases come about, but why they developed in the first place.
Works Cited:
1. Campbell, Neil A., and Jane B. Reece. Biology AP Edition. Upper Saddle River: Prentice Hall College Div, 2004. Print.
2. Moalem, Sharon, and Jonathan Prince. Survival of the Sickest. New York: William Morrow, 2007. Print.
Post #2
“Cholesterol is required to make and maintain cell membranes. It helps the brain to send messages and the immune system to protect us against cancer and other diseases. It’s a key building block in the production of estrogen and testosterone and other hormones” (Moalem 51).
Cholesterol is a type of steroid, which by definition, is a “lipid characterized by a carbon skeleton consisting of four fused rings” (1). Relating to the fluid mosaic model that we learned about in the beginning of the year, one of its main functions is to maintain membrane fluidity at different temperatures. It reduces membrane fluidity by decreasing phospholipid movement at moderate temperatures, but also hinders solidification by disrupting the packing of phospholipids at low temperatures (1). For this reason, cholesterol is a vital component of animal cell membranes.
Cholesterol also has a crucial role in the endocrine system. Since cholesterol is a lipid, it is hydrophobic and can easily diffuse through the phospholipid bilayer of a plasma membrane. Once it enters the target cell, it binds to an intracellular receptor either in the cytoplasm or nucleus. Typically, the hormone-receptor complex acts as a transcription factor and activates the expression of certain genes. The process is summarized in the diagram below (2):
In order for the hormone to create a protein, transcription and translation must occur. In transcription, the DNA molecule unwinds and, using one of the DNA strands as a template, RNA polymerase creates a complementary strand of RNA. It does so by pairing the nucleotides A=U, T=A, G=C and C=G. After, the new RNA strand is transported from the nucleus to a ribosome. In translation, each sequence of three nucleotides is grouped into a codon. tRNA molecules, each with a complementary anti-codon, retrieve the appropriate amino acid from the cytoplasm and carry it to the ribosome. This is done for each codon until a stop codon is reached, and a peptide is formed. The peptide is then released into the cytoplasm (1).
This excerpt connects to the theme of the relationship of structure to function. As mentioned before, cholesterol is a lipid and is hydrophobic. Therefore, it is able to cross the hydrophobic layer of a target cell’s plasma membrane. Cholesterol’s ability to penetrate the plasma membrane of a target cells allows it to serve as a precursor for multiple other hormones in the endocrine system. In addition, the receptor that a lipid-based hormone binds to is shape-specific. As a result, only specific hormones can bind to the receptors (1).
In Chapter 3, Dr. Sharon Moalem discusses the connection between sunlight and cholesterol. It makes sense that he does not go into very much detail regarding the specifics of cholesterol, because that would detract from his point. He presents strong evidence that high cholesterol found in African Americans is an evolutionary adaptation that is no longer needed, but the end of his chapter really bothers me. He states, “If you knew that you might be able to reduce your excess cholesterol by getting enough sunlight to convert it to vitamin D, wouldn’t you rather hit the tanning salon before starting a lifetime of Lipitor?” (Moalem 70). He supports this statement by stating that cholesterol-reducing drugs, such as Lipitor, can have serious side effects. When I researched this, however, I learned that serious side effects are extremely rare, and that drugs such as Lipitor generally cause more good than they do harm (4). At the same time, indoor tanning has a direct link to the premature development of skin cancer, and its effects can be devastating (3). So no, actually. I would rather have high cholesterol at the age of fifty than die of skin cancer before I turn seventeen.
Works Cited
1. Campbell, Neil A., and Jane B. Reece. Biology AP Edition. Upper Saddle River: Prentice Hall College Div, 2004. Print.
2. "Cell Communication Processes in Biology." University of Miami. Web. 02 June 2010. <http://www.bio.miami.edu/~cmallery/150/memb/cellcomm.htm>.
3. "Effects of Tanning Beds." Vanderbilt University. Web. 02 June 2010. <http://www.vanderbilt.edu/AnS/psychology/health_psychology/Tanning.html>.
4. Mayo Clinic. "Statin Side Effects." Mayo Clinic. Web. 02 June 2010. <http://www.mayoclinic.com/health/statin-side-effects/my00205>.
5. Moalem, Sharon, and Jonathan Prince. Survival of the Sickest. New York: William Morrow, 2007. Print.
Commentary 1 (H.K.)
I agree with Margaret's statement about cholesterol-lowering drugs not having as serious side effects on the people that consume them. For example, I know my cousin has been taking the drug Niacin, which lowers the LDL (bad cholesterol) and raises the HDL (good cholesterol), and has experienced no side effects what so ever of this drug. Even though though Niacin has minor side effects like itching of skin and headaches, my cousin has not been affected by any of them. There are many other drugs out there designed to lower cholesterol, who people claim to be are really "dangerous" to the health because of their serious side effects. But the chances of one experiencing the side effects is very low, and it would be a smart idea to take the drug to improve ones health then to worry about it's side effects which rarely occur.
Commentary 1 (KB)
I also think that it is interesting that something that is so useful in so many ways (cholesterol is a key building block and a staple in cell structure) has such a bad reputation. Excess cholesterol is definitely a problem, but I think that Moalem is looking at it the wrong way. My dad's been on Lipitor for a while (high cholesterol/heart problems run on both sides of my family) with no side effects, so I agree with Margaret and Hira that side effects are very rare. However, a recent issue of 17 Magazine did a spread on tanning and using a tanning bed once could increase your risk for melanoma by 75%! (1) But at least you'll be cholesterol free, and have enought vitamin D.
The point I'm trying to make is that there are tradeoffs with everything in life and simply going tanning is a friviolous and dangerous way to suggest that people limit their cholesterol. There are other, safer ways to do it--limiting unhealthy food, getting healthy sun exposure (perhaps while outside exercising) and when genetics really are stacked against you, medicine should be between you and your private physician, not someone who's just writing a book. Different medicines work differently for people (as Dr. Moalem stated in the chapter on methylation) and therefore side effects manifest themselves differently. And lots of the side effects on commericals (severe dehydration, dizziness, loss of limbs, maybe even death) are really probably put in there by lawyers trying to cover themselves in the event that a doctor misprescribes something, or the medicine really does disagree with the patient. Using a medicine correctly when there is a legitimate need should never be frowned upon, especially by a doctor who doens't know the patient's medical history. My dad's uncle died at fifty from a heart attack. And who knows? Maybe Lipitor (along with diet/exercise) is what kept him from having one, too.
Works Cited
"The Tan You Could Be Risking Your Life For." Seventeen May 2010: 80. Print.
Post #3
“The gene that is responsible for G6PD protein production – or deficiency – goes by the same name, G6PD. Because the gene for G6PD deficiency is carried on the X chromosome, the condition is much more common in men… There are more than 100 possible mutations of this gene, but they fit into two major categories, one that arose in Africa, called GdA-, and one that arose around the Mediterranean, called GdMed. These mutations cause serious problems only when free radicals start overwhelming your red blood cells and there isn’t enough G6PD to clean them up” (Moalem 75-76).
In mammals, there are two types of sex chromosomes: X and Y. Humans with two X chromosomes (XX) are female, and humans with one X and one Y chromosome (XY) are male. During meiosis, the two sex chromosomes separate and each gamete receives one. Therefore, each ovum contains an X chromosome, while each sperm can contain either an X or a Y chromosome. When fertilization occurs, the zygote receives one X chromosome from its mother and either an X or Y chromosome from its father. As a result, mothers can pass X-linked alleles to their daughters (XX) and sons (XY), and fathers can pass X-linked alleles only to their daughters (XX). In the case of the G6PD, the gene that is responsible for the G6PD-deficiency is a recessive X-linked gene. This means that females must have two mutated X chromosomes to have a G6PD-deficiency, while males only need one mutated X chromosome (1). Consequently, males are much more likely to exhibit a G6PD-deficiency.
Mutations can arise from base substitutions and gene rearrangements. Also known as point mutations, base substitutions occur when one nucleotide base is substituted for another. They can result in nonsense mutations, which cause the premature termination of protein translation; missense mutations, in which a codon is altered and produces a different amino acid; and silent mutations, which cause no detectable change in the corresponding protein sequence. In addition to that, there are five main types of gene rearrangements:
1. A deletion occurs when a chromosomal segment is lost
2. An insertion occurs when a segment is inserted into the chromosome
3. A duplication occurs when a segment is repeated
4. An inversion occurs when a segment reverses within a chromosome
5. A translocation occurs when a segment is moved from one chromosome to a nonhomologous chromosome. In a reciprocal translocation, the nonhomologous chromosomes exchange fragments. In a nonreciprocal translocation, a chromosome loses a fragment without receiving a fragment in return.
More often than not, a chromosomal alteration changes the protein sequence, which changes the expression of a certain gene (1). These events can give rise to mutations such as the G6PD-deficiency gene.
The theme of continuity and change states that all living things pass down genetic information between generations to maintain the species, but there are mechanisms that can lead to change over time. It connects to the excerpt in the way that the G6PD-deficiency gene has been passed from generation to generation on the X chromosome. While males are more likely to have a G6PD deficiency, females can serve as carriers. Also, mutations resulting from base substitutions or gene rearrangements can lead to mutations such as the G6PD-deficiency gene.
Something I thought was very interesting about this chapter (IV: Hey Bud, Can You Do Me a Fava?) was that many plants that I consume have toxins in them. Dr. Sharon Moalem states, “What’s more surprising is why we continue to cultivate and consume thousands of plants that are toxic to us. The average human eats somewhere between 5,000 and 10,000 natural toxins every year. Researchers estimate that nearly 20 percent of cancer-related deaths are caused by natural ingredients in our diet” (Moalem 83). Somewhat recently, natural and organic food has been gaining popularity. I found it surprising to learn that the “healthy” foods can actually be harmful; for example, the psoralen found in celery can cause skin damage (Moalem 87). I guess it could have been expected, since plants must have evolved defenses to protect themselves from predation, but I still find it rather depressing.
Works Cited:
1. Campbell, Neil A., and Jane B. Reece. Biology AP Edition. Upper Saddle River: Prentice Hall College Div, 2004. Print.
2. Moalem, Sharon, and Jonathan Prince. Survival of the Sickest. New York: William Morrow, 2007. Print.
Post #4
“Most of these microbes are found in the digestive system, where they play crucial roles. These intestinal bacteria, or gut flora, help to create energy by breaking down food products we otherwise couldn’t break down; they help to train our immune systems to identify and attack harmful organisms; they stimulate cell growth; and they even protect us against harmful bacteria” (Moalem 98).
The large intestine of a human is mainly responsible for the reabsorption of water, and is one of the last stages of the digestive process. However, it also contains approximately 100 trillion microorganisms. These microorganisms are mostly harmless bacteria, and live on unabsorbed organic material in the large intestine. Some of the bacteria produce vitamins - such as biotin, folic acid, and vitamin K – that are absorbed into the blood to supplement our dietary intake of vitamins (1). Other bacteria digest polysaccharides for which we have no enzymes, and stimulate the development of the adaptive immune system (2).
Symbiosis is defined as “an ecological relationship between organisms of different species that are in direct contact” (2). It can exist in various forms. In mutualism, both symbiotic organisms benefit. This excerpt provides an excellent example of mutualism; the bacteria living in the digestive system synthesize vitamins, digest polysaccharides, and stimulate the development of the adaptive immune system (1). In return, they are provided with food. In this way, both organisms are able to benefit from the relationship.
In commensalism, one organism benefits while the other is neither helped nor harmed. For example, remoras form temporary attachments onto sharks. When the shark feeds, the remoras consume the scraps. The shark is unaffected by this relationship.
In parasitism, one organism benefits at the expense of the other. A parasite is an organism that “lives on or in the body of another organism (the host), from whose tissues it gets its nourishment and to whom it does some damage” (2). The parasite is able to harm its host either by consuming its tissues or liberating toxins. In addition, the relationship between a parasite and its host can range from “hit and run,” in which the parasite lives in the host for a brief period before moving on to another, and parasites that establish chronic infections. For animals, parasites can come in the form of viruses, bacteria, fungi, protozoans, flatworms, nematodes, insects (e.g. lice) and arachnids (mites) (2).
This excerpt connects to the theme of interdependence in nature. As symbiosis demonstrates, living organisms rarely exist alone in nature. In the case of the intestinal bacteria found in humans, both organisms are able to benefit from one another. There are countless interactions between species that occur on multiple levels, and symbiosis is just one of them.
Something that I learned from researching this topic was that as by-products of their metabolism, many intestinal bacteria generate gases, including methane and hydrogen sulfide. Then, I was able to recall a song that everyone cool used to sing, and it went along the lines of “BEANS, BEANS, THE MAGICAL FRUIT. THE MORE YOU EAT, THE MORE YOU TOOT…” This led me to wonder: do beans make these bacteria more active, therefore causing people to toot more? It turns out I was right, and I even have a link full of additional fascinating information: http://www.heptune.com/farts.html
Works Cited
1. Campbell, Neil A., and Jane B. Reece. Biology. San Francisco: Pearson, Benjamin Cummings, 2005. Print.
2. "Symbiosis." RCN D.C. Web. 10 June 2010. <http://users.rcn.com/jkimball.ma.ultranet/BiologyPages/S/Symbiosis.html>.
Post #5
“The prospect of programmed aging opens up the door to all kinds of exciting possibilities. Already, scientists are exploring benefits that may be found by turning aging mechanisms off – and by turning them back on. The possibility of short-circuiting telomerase in cancer cells – the enzyme that cancer cells use to make themselves immortal – may lead to powerful new weapons against cancer” (Moalem 191).
The semiconservative model states that when a double helix replicates, each of the two daughter molecules will have one old strand and one newly made strand. DNA replication begins when helicase unwinds the DNA molecule. DNA polymerase binds complementary nucleotide bases to the template strand (Adenine=Thymine, Cytosine=Guanine). However, DNA polymerase can only add nucleotides in a 5’ to 3’ direction (the leading strand). As a result, RNA primase must be used to start Okazaki fragments on the lagging strand, which runs in a 3’ to 5’ direction. For linear DNA, the RNA primer on the lagging strand can be removed but cannot be replaced with DNA. For this reason, repeated rounds of replication produce shorter and shorter DNA molecules (3).
To protect against the possible loss of genes at the end of chromosomes, eukaryotic cells have telomeres. Telomeres are nonsense nucleotide sequences at the end of chromosomes that repeat thousands of times. An enzyme called telomerase catalyzes the lengthening of telomeres after DNA replication to ensure that the gene-containing portion is not removed (2).
Cancer cells generally exhibit abnormally high levels of telomerase activity. Because the telomerase is able to quickly restore telomeres, cancer cells are capable of unlimited cell division. In this way, they are essentially immortal. This relates to the theme of science, technology, and society. Advances in technology have led to the discovery of telomerase, which can be applied to cancer research and other fields. In turn, this will greatly benefit society. It is estimated that 1,529,560 people in the United States will develop cancer in 2010, and new discoveries in science will have an enormous impact on society (1).
In this excerpt, Dr. Sharon Moalem writes that the prospect of telomerase “opens the door to all kinds of exciting possibilities.” He basically says that researchers will be able to kill two birds (aging and cancer) with one stone. The shortening of telomeres is believed to be one of the main causes of aging, because it often leads to apoptosis (also referred to as cell suicide). At the same time, the continuous restoration of telomeres is believed to be one of the main causes of cancer. Without a doubt, it will be difficult to cure one problem without affecting the other, and I believe that Dr. Sharon Moalem oversimplifies the complications associated with telomerase research. It is also possible that he is extremely optimistic.
Works Cited
1. Campbell, Neil A., and Jane B. Reece. Biology. San Francisco: Benjamin Cummings, 2002. Print.
2. "Cancer Statistics for 2010." American Cancer Society. Web. 13 June 2010. <http://www.cancer.org/docroot/stt/stt_0.asp>.
3. "DNA Replication." John Kyrk. Web. 13 June 2010. <http://www.johnkyrk.com/DNAreplication.html>.